Silva Vinícius Rodrigues, Azar Ashraf, Goncalves Edmilson Ricardo, Nascimento Thatiane Cristina de Moura, Buchaim Rogerio Leone, Buchaim Daniela Vieira, de Oliveira Fernando Antonio Antunes, Nassar Carolina Costa, de Camargo Tais Mendes, Caboclo Ricardo Farinasso, da Cunha Marcelo Rodrigues
Center for Life Sciences, Pontifical Catholic University (PUC Campinas), Campinas 13034-685, Brazil.
Postgraduate Program in Health Sciences, Faculty of Medicine of Jundiaí (FMJ), Jundiaí 13202-550, Brazil.
Int J Mol Sci. 2025 Jun 20;26(13):5919. doi: 10.3390/ijms26135919.
Endothelial inflammation and atherosclerosis remain leading drivers of cardiovascular disease, yet the post-transcriptional regulators orchestrating these events are not yet completely understood. In this review, we analyse recent preclinical and clinical studies to dissect microRNA (miRNA)-mediated control of vascular endothelial biology. We describe how miR-181b-5p and miR-223 modulate NLRP3 inflammasome activation and pyroptosis, how miR-615-5p, miR-138, and miR-133a coordinate endothelial nitric oxide synthase (eNOS) activity and nitric oxide bioavailability, and how miR-33a/b, miR-150, and miR-342-3p influence lipid efflux and foam-cell formation in atherogenesis. We also discuss miRNA signatures that correlate with endothelial dysfunction in human cohorts. By integrating mechanistic pathways with emerging biomarker data, this study underscores the relevance of miRNAs as both diagnostic and potential targets in vascular diseases.
内皮炎症和动脉粥样硬化仍然是心血管疾病的主要驱动因素,然而,协调这些事件的转录后调节因子尚未完全明确。在本综述中,我们分析了最近的临床前和临床研究,以剖析微小RNA(miRNA)介导的血管内皮生物学调控机制。我们描述了miR-181b-5p和miR-223如何调节NLRP3炎性小体激活和细胞焦亡,miR-615-5p、miR-138和miR-133a如何协调内皮型一氧化氮合酶(eNOS)活性和一氧化氮生物利用度,以及miR-33a/b、miR-150和miR-342-3p如何影响动脉粥样硬化发生过程中的脂质流出和泡沫细胞形成。我们还讨论了与人类队列中内皮功能障碍相关的miRNA特征。通过将机制途径与新出现的生物标志物数据相结合,本研究强调了miRNA作为血管疾病诊断和潜在靶点的相关性。